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Article: Naringin Attenuates Cerebral Ischemia-Reperfusion Injury Through Inhibiting Peroxynitrite-Mediated Mitophagy Activation

TitleNaringin Attenuates Cerebral Ischemia-Reperfusion Injury Through Inhibiting Peroxynitrite-Mediated Mitophagy Activation
Authors
KeywordsCerebral ischemia-reperfusion injury
Mitophagy
Naringin
Nitrative stress
Peroxynitrite
Issue Date2018
PublisherHumana Press, Inc. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035
Citation
Molecular Neurobiology, 2018, v. 55 n. 12, p. 9029-9042 How to Cite?
AbstractExcessive autophagy/mitophagy plays important roles during cerebral ischemia-reperfusion (I/R) injury. Peroxynitrite (ONOO−), a representative reactive nitrogen species, mediates excessive mitophagy activation and exacerbates cerebral I/R injury. In the present study, we tested the hypothesis that naringin, a natural antioxidant, could inhibit ONOO−-mediated mitophagy activation and attenuate cerebral I/R injury. Firstly, we demonstrated that naringin possessed strong ONOO− scavenging capability and also inhibited the production of superoxide and nitric oxide in SH-SY5Y cells exposed to 10 h oxygen-glucose-deprivation plus 14 h of reoxygenation or ONOO− donor 3-morpholinosydnonimine conditions. Naringin also inhibited the expression of NADPH oxidase subunits and iNOS in rat brains subjected to 2 h ischemia plus 22 h reperfusion. Next, we found that naringin was able to cross the blood-brain barrier, and naringin decreased neurological deficit score, reduced infarct size, and attenuated apoptotic cell death in the ischemia-reperfused rat brains. Furthermore, naringin reduced 3-nitrotyrosine formation, decreased the ratio of LC3-II to LC3-I in mitochondrial fraction, and inhibited the translocation of Parkin to the mitochondria. Taken together, naringin could be a potential therapeutic agent to prevent the brain from I/R injury via attenuating ONOO−-mediated excessive mitophagy.
Persistent Identifierhttp://hdl.handle.net/10722/261815
ISSN
2017 Impact Factor: 5.076
2015 SCImago Journal Rankings: 1.819
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFeng, J-
dc.contributor.authorChen, X-
dc.contributor.authorLu, S-
dc.contributor.authorLi, W-
dc.contributor.authorYang, D-
dc.contributor.authorSu, W-
dc.contributor.authorWang, X-
dc.contributor.authorShen, J-
dc.date.accessioned2018-09-28T04:48:34Z-
dc.date.available2018-09-28T04:48:34Z-
dc.date.issued2018-
dc.identifier.citationMolecular Neurobiology, 2018, v. 55 n. 12, p. 9029-9042-
dc.identifier.issn0893-7648-
dc.identifier.urihttp://hdl.handle.net/10722/261815-
dc.description.abstractExcessive autophagy/mitophagy plays important roles during cerebral ischemia-reperfusion (I/R) injury. Peroxynitrite (ONOO−), a representative reactive nitrogen species, mediates excessive mitophagy activation and exacerbates cerebral I/R injury. In the present study, we tested the hypothesis that naringin, a natural antioxidant, could inhibit ONOO−-mediated mitophagy activation and attenuate cerebral I/R injury. Firstly, we demonstrated that naringin possessed strong ONOO− scavenging capability and also inhibited the production of superoxide and nitric oxide in SH-SY5Y cells exposed to 10 h oxygen-glucose-deprivation plus 14 h of reoxygenation or ONOO− donor 3-morpholinosydnonimine conditions. Naringin also inhibited the expression of NADPH oxidase subunits and iNOS in rat brains subjected to 2 h ischemia plus 22 h reperfusion. Next, we found that naringin was able to cross the blood-brain barrier, and naringin decreased neurological deficit score, reduced infarct size, and attenuated apoptotic cell death in the ischemia-reperfused rat brains. Furthermore, naringin reduced 3-nitrotyrosine formation, decreased the ratio of LC3-II to LC3-I in mitochondrial fraction, and inhibited the translocation of Parkin to the mitochondria. Taken together, naringin could be a potential therapeutic agent to prevent the brain from I/R injury via attenuating ONOO−-mediated excessive mitophagy.-
dc.languageeng-
dc.publisherHumana Press, Inc. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035-
dc.relation.ispartofMolecular Neurobiology-
dc.rightsThe final publication is available at Springer via http://dx.doi.org/[insert DOI]-
dc.subjectCerebral ischemia-reperfusion injury-
dc.subjectMitophagy-
dc.subjectNaringin-
dc.subjectNitrative stress-
dc.subjectPeroxynitrite-
dc.titleNaringin Attenuates Cerebral Ischemia-Reperfusion Injury Through Inhibiting Peroxynitrite-Mediated Mitophagy Activation-
dc.typeArticle-
dc.identifier.emailYang, D: yangdan@hku.hk-
dc.identifier.emailShen, J: shenjg@hku.hk-
dc.identifier.authorityYang, D=rp00825-
dc.identifier.authorityShen, J=rp00487-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s12035-018-1027-7-
dc.identifier.pmid29627876-
dc.identifier.scopuseid_2-s2.0-85045035520-
dc.identifier.hkuros292992-
dc.identifier.volume55-
dc.identifier.issue12-
dc.identifier.spage9029-
dc.identifier.epage9042-
dc.identifier.isiWOS:000448483400019-
dc.publisher.placeUnited States-

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